The long-range objective of our research is to define the role of the inflammatory/immune system in the induction/maintenance/resolution of psoriasis. The immediate objective of our research has been to determine whether or not the skin of patients with psoriasis is inherently disordered. To define this, we have taken advantage of a biologic support system, void of host humoral factors, wherein the usual structural, as well as the differentiation/proliferation features inherent to host human epidermis, persist: the transplantation of human skin to congenitally athymic (nude) mice. We have determined that host skin retains absorptive features, as well as responsive features, to various proliferative agents, i.e., they are the same while on the host, as well as when they have been transplanted to the nude mouse. We have demonstrated that psoriasis skin appears to be inherently defective, i.e., involved skin has a decrease in the labelling index, as a function of time, while on the mouse; uninvolved skin, on the other hand, has an increase in the labelling index as a function of time. This is without the application of irritating agents to the skin, or without host humoral factors being injected. Normal skin does not have similar changes, i.e., there is no increase in epidermal proliferation after transplantation to the nude mouse.